Persistent increases in Ca2+ influx through Cav1.2 shortens action potential and causes Ca2+ overload-induced afterdepolarizations and arrhythmias-Reference-Cited by-同舟云学术

Persistent increases in Ca2+ influx through Cav1.2 shortens action potential and causes Ca2+ overload-induced afterdepolarizations and arrhythmias

Published:2015-11-26 Issue:1 Volume:111 Page:
ISSN:0300-8428
Container-title:Basic Research in Cardiology
language:en
Short-container-title:Basic Res Cardiol

Author:

Zhang Xiaoying,Ai Xiaojie,Nakayama Hiroyuki,Chen Biyi,Harris David M.,Tang Mingxin,Xie Yuping,Szeto Christopher,Li Yingxin,Li Ying,Zhang Hongyu,Eckhart Andrea D.,Koch Walter J.,Molkentin Jeffery D.,Chen Xiongwen

Funder

National Heart, Lung, and Blood Institute

American Heart Association

Publisher

Springer Science and Business Media LLC

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology

Link

http://link.springer.com/content/pdf/10.1007/s00395-015-0523-4.pdf

Reference36 articles.

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2. Anderson ME (2004) Calmodulin kinase and L-type calcium channels; a recipe for arrhythmias? Trends Cardiovasc Med 14:152–161. doi: 10.1016/j.tcm.2004.02.005

3. Antoons G, Sipido KR (2008) Targeting calcium handling in arrhythmias. Europace 10:1364–1369. doi: 10.1093/europace/eun271

4. Barrett CF, Tsien RW (2008) The Timothy syndrome mutation differentially affects voltage- and calcium-dependent inactivation of CaV1.2 L-type calcium channels. Proc Natl Acad Sci USA 105:2157–2162. doi: 10.1073/pnas.0710501105

5. Barry DM, Nerbonne JM (1996) Myocardial potassium channels: electrophysiological and molecular diversity. Annu Rev Physiol 58:363–394. doi: 10.1146/annurev.ph.58.030196.002051

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